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KMID : 0370220220660010007
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Yakhak Hoeji
2022 Volume.66 No. 1 p.7 ~ p.15
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Effect of Baicalin on the LPS-Induced Production of Inflammatory Mediators in Low-Dose Corticosterone Pretreated RAW 267.4 cells and Hepa1c1c-7 Cells
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Chae Byeong-Suk
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Abstract
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Low-dose glucocorticoids (GCs) are known to induce inflammation and immunosuppression. However, whetherpreconditioning with a low dose of GCs induces hepatic inflammation remains unclear. Although baicalin has beneficialtherapeutic activity against liver damage, 100 μM baicalin enhances the lipopolysaccharide (LPS)-induced production ofinflammatory acute-phase proteins in Hepa1c1c-7 cells. This study was performed to investigate the effect of 100 μMbaicalin on the LPS-induced production of inflammatory mediators in liver cells, including Kupffer cells and hepatocytes,pre-conditioned with a low dose of GCs. RAW 267.4 cells and Hepa1c1c-7 cells were pretreated with 50 (cort 50) or 100ng/mL (cort 100) corticosterone for 24 h and then cultured with 100 μM baicalin in fresh complete medium in thepresence of LPS. Our results demonstrated that baicalin markedly decreased the LPS-induced production of TNF-α, IL-6,IL-1β, and nitric oxide in RAW 267.4 cells. Baicalin also strongly attenuated the LPS-induced production of TNF-α incort 50- and cort 100-pretreated RAW 267.4 cells. Baicalin significantly upregulated the production of IL-6 induced byLPS and the production of VEGF decreased by LPS, but decreased the LPS-induced production of CRP in cort 100-pretreated Hepa1c1c-7 cells compared to untreated Hepa1c1c-7 cells. In conclusion, these findings suggest that 100 μMbaicalin may enhance the LPS-induced production of inflammatory acute-phase proteins in hepatocytes, whereas it maydownregulate these protein levels in macrophages and Kupffer cells. Moreover, preconditioning with a low dose ofcorticosterone may prime the effects of 100 μM baicalin on the LPS-induced production of IL-6 in hepatocytes, leadingto hepatic insulin resistance or fatty liver disease.
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KEYWORD
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Corticosterone pretreatment, TNF-α, IL-6, NO, CRP, VEGF, Hepatic inflammation, Baicalin
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